Figure 6.

Enhanced secretion of SNCG exacerbates adipogenesis under conditions of decreased miR‐424(322)/503. A) Knock‐down of γ‐Synuclein (Sncg) in miR‐KO mouse embryonic fibroblasts blunts their enhanced adipogenic commitment, as revealed by gene expression measures in mature adipocytes (MAs; n = 5/group; Tukey's “post‐hoc” tests). B) Schematic representation of recombinant (r)SNCG treatments in human pre/adipocytes. PM‐1, DM‐2, and AM‐1 stand for preadipocyte, adipocyte differentiation, and adipocyte maintenance media, respectively. C) Treatments of rSNCG lasting 14 days enhanced the adipogenic commitment of primary fat precursor cells, as revealed by Oil Red O staining, and either(D) sustained (during the adipogenic course) or E) acute (48‐h exposure in fully‐differentiated adipocytes) treatments dose‐dependently (i.e., 100 and 500 ng mL⁻¹) increased expression signatures suggestive of an altered inflammatory activity. Data are presented as mean ± S.E.M (n > 3/group). Tukey's “post‐hoc” tests were used to determine significant differences versus control). F) Serum SNCG levels in Wt and miR‐KO males and females under NC (n > 6/group; Sudent's t‐test). G) Bean plots show variations in plasma SNCG for non‐obese (BMI<30 kg m⁻²; n = 76, green) and obese (n = 102, red) women and men, and H) in obese patients (n = 19) at the baseline (red) and upon ≈1 years of surgery‐induced weight loss (green). Statistical significance was assessed by paired Student t‐tests (see Table S4, Supporting Information for additional details). *p < 0.05; **p < 0.01; ***p < 0.001. NS, not significant.